Leveraging Natural Variation to Identify New Sources of Resistance to Pseudomonas syringae pv. tomato
Robyn Roberts: Boyce Thompson Institute
<div><em>Pseudomonas syringae </em>pv. <em>tomato </em>(<em>Pst</em>) causes bacterial speck disease of tomato. The only genetic resistance to <em>Pst</em> is conferred by the <em>R</em> gene <em>Pto</em>, which recognizes the <em>Pst</em> effectors AvrPto and AvrPtoB. However, <em>Pst</em> strains have recently emerged lacking these effectors, rendering <em>Pto</em>-mediated resistance ineffective. Our study aims to identify new sources of genetic resistance against <em>Pst</em> that can be introgressed into tomato breeding lines. Using available whole-genome resequencing data, we leveraged natural variation among tomato heirlooms, breeding lines, and a wild species to screen 216 accessions for new sources of resistance. We inoculated the accessions by spraying <em>Pst</em> mutant strains deleted for different effectors and/or flagellin to help elucidate whether observed disease resistance responses involve effector-triggered (ETI) or pattern-triggered (PTI) immune pathways. Interestingly, our screen uncovered new <em>Pst</em> disease phenotypes beyond the typical speck symptoms, and we have found that some of these phenotypes are simply inherited. Using an assay that measures the production of PTI-related reactive oxygen species, we discovered new accessions that have increased, or conversely, no response to the flagellin peptides flg22 or flgII-28, which are recognized by the pattern recognition receptors <u>F</u>LAGELLIN <u>S</u>ENSING <u>2</u> (FLS2) or <u>F</u>LAGELLIN <u>S</u>ENSING <u>3</u> (FLS3), respectively. These results provide a gateway for the study of the molecular mechanisms acting downstream of these two pattern recognition receptors. We are currently using available whole-genome resequencing data and genetic approaches to identify gene candidates that underlie novel resistance or susceptibility to <em>Pst</em>.</div>
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